The regulation of helminth populations tends to occur primarily as a result of limitations imposed on the build up of parasite subpopulations within individual hosts (Anderson & May, 1979; May & Anderson, 1979). Considering the relevance of these factors to the success or otherwise of intestinal helminth control programmes, it is perhaps surprising that more information is not yet available concerning the particular mechanisms which may be responsible, and in particular, the population consequences of the immune responses which such parasites may precipitate.Density-dependence in a single rate parameter, if operative over the naturally observed numerical range, is sufficient to regulate parasite population flow throughout the life-cycle, whether direct or indirect (Anderson, 1976). For the genera given in Table 1, this could be provided by the observed pattern of parasite mortality and/or fecundity. It is of interest to note, however, that circumstantial evidence cited in the Table suggests that each of the 6 genera is also potentially able to induce host mortality under certain conditions. Whether this acts in a density-dependent manner in natural infections is almost entirely unknown. Rapid reproduction may be of great selective advantage to intestinal helminths, even if it is necessarily accompanied by pathogenicity (see Anderson, 1981). If the manner in which this pathogenicity acts in any way enhances the stability of the host-parasite interaction, then perhaps it may have contributed to the selection pressures which have led so many genera to continue to break the rules of the ‘well-adapted’ parasite (see, for example, Noble & Noble, 1971).